1. NICOTINIC ANTAGONIST
1.1. What is it?
1.1.1. compounds that bind to cholinergic nicotinic receptors with no intrinsic efficacy
1.1.2. Nicotinic receptors
1.1.2.1. Nm - muscle type
1.1.2.1.1. located at the skeletal muscle end plates
1.1.2.1.2. stimulate skeletal muscle contraction
1.1.2.1.3. MOA: post-synaptic and excitatory
1.1.2.1.4. Agonist: ACh, CCh, suxamethonium, PTMA
1.1.2.1.5. Antagonist: pancuronium
1.1.2.2. Nn - Ganglion type
1.1.2.2.1. located at the autonomic ganglia of all type
1.1.2.2.2. for depolarization and postganglionic impulse
1.1.2.2.3. MOA: excitatory
1.1.2.2.4. Agonist: ACh, CCh, nicotine, DMPP
1.1.2.2.5. Antagonist: mecamylamine, trimetaphan
1.1.3. Subclasses
1.1.3.1. Skeletal neuromuscular blocking agents
1.1.3.2. Ganglionic blocking agents
1.2. NMJ Blockers
1.2.1. Non-depolarizing competitive antagonist
1.2.1.1. Pancuronium bromide
1.2.1.1.1. Pharmacokinetics
1.2.1.1.2. Pharmacodynamics
1.2.1.1.3. CI
1.2.1.1.4. Side effect
1.2.2. Depolarizing agonist
1.2.2.1. Suxamethonium chloride (succinylcholine)
1.2.2.1.1. Pharmacokinetics
1.2.2.1.2. Pharmacodynamics
1.2.2.1.3. CI
1.2.2.1.4. Side effect
2. MUSCARINIC ANTAGONIST
2.1. What is it?
2.1.1. agent that has high binding affinity for muscarinic receptor, but no intrinsic activity
2.1.2. reversible competitive antagonist
2.1.3. aka anticholinergics, antimuscarinics, cholinergic blockers, antispasmodics, parasympatholytics
2.2. Drugs
2.2.1. Natural
2.2.1.1. Atropine
2.2.1.1.1. Pharmacokinetics
2.2.1.1.2. Pharmacodynamics
2.2.1.1.3. Uses / CI
2.2.1.2. Scopolamine
2.2.1.2.1. Pharmacokinetics
2.2.1.2.2. Pharmacodynamics
2.2.2. Synthetic
2.2.2.1. Ipratropium bromide
2.2.2.1.1. Blocks cholinergic bronchiole constriction - allows bronchiole dilation to overcome pulmonary constriction
2.2.2.1.2. Uses / CI
2.2.2.1.3. Adverse effects
2.2.2.2. Tiotropium bromide
2.2.2.2.1. Same MOA and CI as ipratropium bromide
2.2.2.2.2. Adverse effects